The leaflets of atrioventricular valves (mitral and tricuspid) are thin, diaphanous structures that rely on a system of long, thin, cord-like supports to maintain competence of the valve in the loaded condition. These supports are appropriately termed the chordae tendinae, and attach the papillary muscles to the valve leaflets.
Mitral valve dysfunction can be broadly grouped into four categories. Type I has normal leaflet motion, but regurgitation arises from annular dilation, or more rarely, leaflet perforation. Type II displays excessive leaflet motion and is commonly termed prolapse. It is the condition in which one or both leaflets are misaligned, and it arises from chordae tendinae or papillary muscle stretching or degeneration. Type IIIa leaflets have normal alignment but reduced motion due to thickening of the leaflet(s) or subannular structures. Type IIIb is a consequence of ventricular dilation. As the ventricle dilates, the papillary muscles are displaced laterally causing leaflet tethering and subsequent regurgitation.
When the chordae tendinae degenerate and become stretched, leaflet prolapse can arise and the leaflet(s) can misalign under systolic loading.
Atrioventricular valve prolapse is a common cardiac disease; in most cases, it is asymptomatic, but when the leaflet misalignment becomes severe enough, regurgitation results. In the majority of cases, the regurgitation arises from a misalignment of the leaflets in which one of the leaflets displaces to a position superior to the other, allowing flow to bypass the leaflets, but the misalignment can also be the result of two prolapsed leaflets. To illustrate, a side cross-sectional view of a normal valve 5a is shown in FIG. 1A, a valve 5b with one prolapsed leaflet 7 due to dysfunctional chordae tendinae 6 in FIG. 1B, and a valve 5c with two prolapsed leaflets 7 in FIG. 1C.
Heretofore, when the atrioventricular valves required replacement, the leaflets were excised, and commonly, the same prostheses as used for the semilunar valves, either mechanical or bioprosthetic implanted, despite the low-profile nature of the AV valves. This approach, though it has met with some success, ignores the unique anatomy/pathology of the AV valves.
In recent years, mitral valve repair has shown initial good success, but it is an extremely invasive and complicated procedure, typically performed only in university hospitals. Leaflet resection involves cutting out the extra tissue and sewing the remnants back together, cardiopulmonary bypass is required, and experience has shown that the initial good result does not necessarily persist. Another procedure of similar complexity is to replace stretched or broken chordae tendinae with suture of expanded polytetrafluoroethylene (ePTFE). Thus, new ways of improving or restoring native valve function is needed.